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Striatal cholinergic interneurons: their depletion and its progression.

Abudukeyoumu N, Garcia-Munoz M, Jaidar OP, Arbuthnott G (2016) Striatal cholinergic interneurons: their depletion and its progression. Neuroscience 2016 Abstracts 245.09 / RR4. Society for Neuroscience, San Diego, CA.

Summary: Even before the discovery that Parkinson’s was produced by the loss of dopaminergic neurons, this neurological disease was treated with anticholinergic drugs. A balance between cholinergic and dopaminergic activity in striatum is not only important in PD but for the normal function of the nucleus (i.e., behavior, reward, memory and cognitive functions). An important source of striatal acetylcholine (Ach) comes from giant and sparsely distributed cholinergic interneurons (ChI). However, their study has been hampered by a concentration of only 1-3 % of the whole striatal cell population. We performed a stereological systematic random sampling of striatal tissue from 21 days old C57BL/6J male mice. To selectively deplete ChI we performed a stereotaxic injection of saporin ribosome inactivating immunotoxin that targets choline acetyltransferase (0.3µl). Following survival periods of 2, 4 or 6 weeks, animals were sacrificed and brain sections immunostained against ChAT to identify ChI, or against vesicular acetylcholine transporter (vAChT) to identify synaptic boutons. For each of the three survival periods, we counted and compared the number of ChIs between the intact and the lesioned hemispheres and the change in the number of vesicular acetylcholine transporters (vAChT). Compared to striatal sections from naïve controls and sham injections, we observed a decrease in ChIs according to each survival period of 24.4% (week 2, n=9), 33.74% (week 4, n= 11) and 19.89% (week 6, n=10). In contrast, we observed a percent increase in vAChT positive boutons of 42.3, 21.6 and 28.3% for each of the respective survival periods (n=9, n=11 and n=10). We are investigating whether the increase in vAChT positive terminals is due to an indirect upregulation produced by compensatory axonal sprouting from surviving ChI, or from afferent axonal terminal fields of cholinergic mesopontine neurons.

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